Pathophysiology of heart failure: neuroendocrine response

The understanding of the pathophysiology of heart failure is an emerging science. Although the mortality rate remains high, there has been some improvement in treatment in recent years. What was once thought to be a purely hemodynamic disorder now is understood to be a disease of cellular pathophysiology. The progression of compensated ventricular dysfunction to symptomatic heart failure is marked by the activation of vasoconstrictor hormones. Norepinephrine, renin-angiotensin-aldosterone, and arginine vasopressin are secreted in response to inadequate systemic perfusion. These combine to increase preload and afterload on an already failing heart. Baroreceptor function is attenuated, allowing for the continued sympathoexecitatory state. In addition, local tissue factors mitigate against a return to normal ventricular function by down-regulation of beta receptors, stimulation of local vasoconstrictor hormone secretion, and promotion of growth. Patients in intensive care units with chronic heart failure are best managed with an understanding of how their altered physiology affects their clinical presentation.